2002
DOI: 10.1016/s0006-291x(02)02666-9
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Starvation-induced posttranscriptional control of rat liver mitochondrial citrate carrier expression

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Cited by 24 publications
(31 citation statements)
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“…The absence of a consistent difference in the transcriptional rates due to the dietary treatment suggested that Cic gene regulation occurred by a post-transcriptional mechanism. In particular, this study confirmed that the reduced CiC mRNA abundance observed in starved rats could be ascribed to its shorter half-life, suggesting that starvation accelerates the degradation of CiC mRNA (59). The reduced CiC activity in starved animals gradually increased upon refeeding, reaching fed-rat values 6-9 h following refeeding.…”
Section: Starvation and Refeedingsupporting
confidence: 80%
See 1 more Smart Citation
“…The absence of a consistent difference in the transcriptional rates due to the dietary treatment suggested that Cic gene regulation occurred by a post-transcriptional mechanism. In particular, this study confirmed that the reduced CiC mRNA abundance observed in starved rats could be ascribed to its shorter half-life, suggesting that starvation accelerates the degradation of CiC mRNA (59). The reduced CiC activity in starved animals gradually increased upon refeeding, reaching fed-rat values 6-9 h following refeeding.…”
Section: Starvation and Refeedingsupporting
confidence: 80%
“…These findings suggested that the starvation-induced decrease of CiC activity could be ascribed to modifications of the intrinsic properties of CiC. In fact, a subsequent study showed a considerable reduction ( 40%) of CiC mRNA abundance in starved rats when compared with fed animals (59). The absence of a consistent difference in the transcriptional rates due to the dietary treatment suggested that Cic gene regulation occurred by a post-transcriptional mechanism.…”
Section: Starvation and Refeedingmentioning
confidence: 95%
“…Similar changes were observed in ANIT, carbon tetrachloride, and hydrazineinduced hepatotoxicity (Wu et al, 2005). The reduced organic acid levels suggested that oxidative phosphorylation was inhibited, glycolysis was increased (Siculella et al, 2002;Connor et al, 2004), and that exposure to PCBs and TCDD affected the mitochondrial energy metabolism in liver, although the effect of other factors could not be excluded. The level of glucose in the urine was increased significantly in all treatment groups, which suggested that the rates of gluconeogenesis and glycolysis increased because the lipid metabolism in these animals failed.…”
Section: Discussionmentioning
confidence: 57%
“…TCC has been extensively characterized in liver mitochondria from mammals and fish (for review, see [11]). A parallel decrease of TCC activity and lipogenesis in the liver of starved [12] and n 脌 6 PUFA-fed rats was reported [13]. The aim of this study was to investigate whether diets with different fatty acid compositions, i.e., rich in either long chain saturated fatty acids (BT) or monounsaturated fatty acids (OO) or n 脌 3 PUFA (FO) could influence the hepatic TCC expression and, if so, to characterize the molecular mechanism responsible for TCC gene regulation.…”
Section: Introductionmentioning
confidence: 90%
“…The RNA blots were hybridized with rat liver TCC cDNA probe as reported by Siculella et al [12]. For normalization of the hybridization signals, the same membranes were hybridized using a probe encoding part of the human b-actin.…”
Section: Isolation Of Rna and Northern Blot Analysismentioning
confidence: 99%